The participation of an endogenous protein activator in the process of adenylate cyclase supersensitivity to endogenous activators was studied. "Chemical denervation" supersensitivity of striatal dopamine receptors was obtained after discontinuation of chronic treatment with antipsychotics. Animals treated with the cataleptogenic antipsychotics, haloperidol and (plus)-butaclamol had an amount of the activator in their striatal membranes larger than control rats and the adenylate cyclase activity was more susceptible to DA stimulation than that of control animals. However, rats treated with the non-cataleptogenic clozapine or (minus)-butaclamol which is inactive as an antipsychotic had no change in striatal activator content or in the susceptibility of adenylate cyclase to DA stimulation. It is possible that the adenylate cyclase super-sensitivity could be accounted for by the increase in the activator protein in the striatal membranes.